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Biomedical subjects

R A Meyer

Publications and source records attributed to R A Meyer.

At least 19 recordsLinked to original sources
PubMed1992

Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and impact of overweight.

OBJECTIVES: This study was designed to determine the most appropriate method to normalize left ventricular mass for body size. BACKGROUND: Left ventricular mass has been normalized for body weight, surface area or height in experimental and clinical studies, but it is uncertain which of these approaches is most appropriate. METHODS: Three normotensive population samples--in New York City (127 adults), Naples, Italy (114 adults) and Cincinnati, Ohio (444 infants to young adults)--were studied by echocardiography. Relations of left ventricular mass to body size were similar in all normal weight groups, as assessed by linear and nonlinear regression analysis, and results were pooled (n = 611). RESULTS: Left ventricular mass was related to body weight to the first power (r = 0.88), to body surface area to the 1.5 power (r = 0.88) and to height to the 2.7 power (r = 0.84), consistent with expected allometric (growth) relations between variables with linear (height), second-power (body surface area) and volumetric (left ventricular mass and body weight) dimensions. Strong residual relations of left ventricular mass/body surface area to body surface area (r = 0.54) and of ventricular mass/height to height (r = 0.72) were markedly reduced by normalization of ventricular mass for height2.7 and body surface area1.5. The variability among subjects of ventricular mass was also reduced (p < 0.01 to p < 0.002) by normalization for body weight, body surface area, body surface area1.5 or height2.7 but not for height. In 20% of adults who were overweight, ventricular mass was 14% higher (p < 0.001) than ideal mass predicted from observed height and ideal weight; this increase was identified as 14% by left ventricular mass/height2.7 and 9% by ventricular mass/height, whereas indexation for body surface area, body surface area1.5 and body weight erroneously identified left ventricular mass as reduced in overweight adults. CONCLUSIONS: Normalizations of left ventricular mass for height or body surface area introduce artifactual relations of indexed ventricular mass to body size and errors in estimating the impact of overweight. These problems are avoided and variability among normal subjects is reduced by using left ventricular mass/height2.7. Simple nomograms of the normal relation between height and left ventricular mass allow detection of ventricular hypertrophy in children and adults.

Adult↗
PubMed1992

Craniometric measurements of craniofacial malformations in the X-linked hypophosphatemic (Hyp) mouse on two different genetic backgrounds: C57BL/6J and B6C3H.

This study reports data on craniometric measurements in the X-linked hypophosphatemic (Hyp) mouse on two different genetic backgrounds: C57BL/6J and B6C3H. Heads of normal females "+/+," normal males "+/Y," heterozygous mutant females "Hyp/+," and hemizygous mutant males "Hyp/Y" for each genetic background were examined. Data were collected via skull measurements. On a C57BL/6J background, the neurocranium of mutants "Hyp/+" and "Hyp/Y" was shorter and slightly higher than in normal counterparts. On a B6C3H background, mutant mice "Hyp/+" and "Hyp/Y" were shorter in neurocranial length than in normal counterparts. Viscerocranial height was larger in "Hyp/Y" than in normal counterparts. No differences in neurocranial and mandibular height were found. Mutant mice on a C57BL/6J background were compared to mutant mice on a B6C3H background. No differences in neurocranial length were found. Cranial length was shorter in "Hyp/Y" on C57BL/6J than in "Hyp/+" on B6C3H. Facial length parameters were shorter in "Hyp/Y" on C57BL/6J than in "Hyp/Y" and "Hyp/+" mutant mice on B6C3H. Mandibular length was shorter in "Hyp/Y" on C57BL/6J than in "Hyp/+" on C57BL/6J and both mutant mice ("Hyp/Y" and "Hyp/+") on a B6C3H background. The results of this study indicate that craniofacial growth is less affected in mutant mice on a B6C3H genetic background than in mutant mice on a C57BL/6J genetic background.

Animals↗
PubMed1992

Donor site morbidity of greater auricular nerve graft harvesting.

To better understand the risks of obtaining greater auricular nerve (GAN) grafts, a retrospective analysis of 29 patients who underwent GAN graft procurement between 1985 and 1990 was conducted. No short-term morbidity was noted. Thirteen patients developed symptomatic nerve injuries, of which 6 reported spontaneous resolution in an average of 4.6 months. Three patients developed neuromas and 1 formed a hypertrophic scar. Persistent nerve injury symptoms were well tolerated in all but one patient, who developed sympathetic-mediated pain.

Adolescent↗
PubMed1992

Peripheral and central mechanisms of cutaneous hyperalgesia.

Hyperalgesia after cutaneous injury can be divided into two phenomena: Primary hyperalgesia occurs at the site of injury and is characterized by hyperalgesia to mechanical and heat stimuli. Secondary hyperalgesia occurs outside the injury site and is characterized by mechanical hyperalgesia only. Hyperalgesia in inflammatory processes corresponds to primary hyperalgesia. Hyperalgesia in referred pain and neuropathic pain resembles secondary hyperalgesia (Table 3). Evidence for the latter would be strengthened if hyperalgesia to cooling stimuli, which is observed in neuropathic pain, was also demonstrated in referred pain and in secondary hyperalgesia. Some of the more likely neural mechanisms to explain primary and secondary hyperalgesia are illustrated in Fig. 8. Primary hyperalgesia to heat stimuli has a counterpart in the sensitization of peripheral nociceptors to heat stimuli (Fig. 8A), leading to similar changes in central neurons. In addition, the enlargement of the mechanical receptive field of primary afferent nociceptors to include the site of injury may account for the primary hyperalgesia to mechanical stimuli (Fig. 8B). In the literature, there are some contradictions with respect to the stimulus modalities to which hyperalgesia and sensitization occur. In spite of the well-documented sensitization of primary afferent nociceptors to heat stimuli, there are few studies on its molecular mechanisms. On the other hand, there is pharmacological evidence for a peripheral mechanism of primary mechanical hyperalgesia, but little direct evidence that nociceptors can be sensitized to mechanical stimuli by injury. This contradiction should spawn further investigations into the mechanical response properties of nociceptors and into the molecular mechanisms of heat sensitization. Secondary hyperalgesia to mechanical stimuli is likely due to the sensitization of central pain signalling neurons (CPSNs). This sensitization could involve only input from nociceptors (Fig. 8C), since mechanical pain thresholds after a cutaneous injury are of the same order as those of nociceptors. Central sensitization could also be the result of enhanced connectivity between low-threshold mechanoreceptors and CPSNs (Fig. 8D). This form of sensitization may account for the pain to light touch associated with neuropathic pain. Receptive field plasticity is a prevalent property of dorsal horn neurons and probably plays a vital role with regard to hyperalgesia. The molecular mechanisms of synaptic plasticity are currently subject to intense experimental investigation and may provide new insights on the mechanisms of pain and hyperalgesia.

Animals↗
PubMed1992

Human in situ dosimetry: differential insertion loss during passage through abdominal wall and myometrium.

We constructed a specialized in vivo exposimetry system and determined selected ultrasonic field quantities. We examined two groups of non-pregnant women (nulliparas = 14, multiparas = 9) under conditions of full and empty bladder. A calibrated 7-element linear array hydrophone was placed in the anterior fornix of the vagina in each subject. In the full bladder condition, the sound beam traversed the anterior abdominal wall and full bladder, whereas after voiding, the sound beam traversed the abdominal wall and anteverted uterine fundus. Each study was conducted using a 3.5 MHz mechanical sector transducer. Calibration data were recorded after completion of each in vivo experiment. Data from both groups were pooled for analysis. Assuming (1) the sound path through the full bladder is loss less, the insertion loss (ILFULL) should represent the insertion loss for the abdominal wall (ILABD WALL) 8.2 +/- 5.6 dB; whereas (2) for the empty bladder condition, (ILEMPTY) represents (ILABD WALL+ILUTERUS). Subtracting ILFULL from ILEMPTY yields ILUTERUS = 5.8 +/- 6.8 dB. Therefore, knowing the respective path lengths and normalizing for frequency, the mean tissue attenuation coefficients (A) are estimated to be AABD WALL = 1.39 dB/cm-MHz and AUTERUS = 0.14 dB/cm-MHz. These attenuation data suggest that the abdominal wall is the principal source of ultrasonic energy loss.

Abdominal Muscles↗
PubMed1992

Left ventricular mechanics in the preterm infant and their effect on the measurement of cardiac performance.

The effects of the transition from fetal to postnatal circulation on left ventricular geometry, wall motion, and echocardiographic measurements of function in the human preterm infant are largely unknown. To determine whether abnormalities in left ventricular geometry are present in the normal preterm infant after birth and, if so, for how long, and to examine possible contributing factors and their effect on the measurement of cardiac performance, we obtained serial echocardiograms of 14 healthy preterm infants (gestational age, 33 +/- 2 weeks; birth weight, 1940 +/- 470 gm) at 9.5 +/- 3.5 days of age (time 1) and again at 51 +/- 16 days (time 2). Left ventricular shape and wall motion were measured and estimates of wall stress and mass were made. Performance was assessed by standard M-mode shortening fraction and by transverse two-dimensional area shortening. At time 1 septal flattening caused distortion of left ventricular shape. As the patients grew older, septal flattening resolved and the left ventricle tended to assume a circular cross-sectional shape. Wall-motion analysis demonstrated poor motion of the midseptum and anterior free wall at time 1, which improved at time 2 (p = 0.06). Left ventricular mass increased from 24 +/- 5 to 41 +/- 7 gm/m2 (p = 0.0001) and wall stress decreased from 49 +/- 21 to 38 +/- 13 gm/cm2 (p = 0.005) between time 1 and time 2. Shortening fraction was lower at time 1 than at time 2 (18% +/- 7% vs 28% +/- 8%; p = 0.001; normal limit = 28% to 45%); however, there was no significant difference in area shortening between time 1 and time 2 (49% +/- 10% vs 53% +/- 8%; normal limit = 45% to 65%). We conclude that the preterm newborn infant has distorted left ventricular shape and abnormal wall motion, which alter measurements of shortening fraction and persist for the first weeks of life. Area shortening may be necessary to assess left ventricular performance during the first weeks of life in the premature infant.

Echocardiography↗
PubMed1992

Role of kinins in pain and hyperalgesia: psychophysical studies in a patient with kininogen deficiency.

1. Bradykinin is considered to be an important mediator of pain and hyperalgesia associated with injury and inflammation. Psychophysical studies were conducted in a patient with complete kininogen deficiency to determine whether the absence of bradykinin was associated with abnormalities in pain sensibility. Pain evoked by heat stimuli to the thenar eminence was tested before and after a localized burn, which has been shown to cause hyperalgesia in normal subjects. In addition, pain evoked by intradermal administration of bradykinin (0.1-10 micrograms) to the forearm and the effects of bradykinin on pain induced by heat stimuli were studied. The patient rated the intensity of pain evoked by all heat stimuli relative to the pain induced by a 3 s 45 degrees C stimulus. 2. The patient's heat pain threshold (45 degrees C) in the glabrous skin was similar to that of age-matched control subjects (n = 5) and to that previously observed in younger control subjects. 3. The burn resulted in a decrease in pain threshold and an increase in pain induced by suprathreshold stimuli. The magnitude of hyperalgesia was within the range observed in the age-matched control subjects and in younger control subjects. Thus, kinins are not essential for the development of hyperalgesia after heat injury. 4. In control subjects, intradermal injections of bradykinin produced pain and hyperalgesia to heat stimuli. In the patient, intradermal bradykinin injections induced minimal pain and no hyperalgesia to heat stimuli. Thus, congenital absence of kininogens may be associated with a deficiency in bradykinin receptors.

Aged↗
PubMed1992

Inhibition of gap junction and adherens junction assembly by connexin and A-CAM antibodies.

We examined the roles of the extracellular domains of a gap junction protein and a cell adhesion molecule in gap junction and adherens junction formation by altering cell interactions with antibody Fab fragments. Using immunoblotting and immunocytochemistry we demonstrated that Novikoff cells contained the gap junction protein, connexin43 (Cx43), and the cell adhesion molecule, A-CAM (N-cadherin). Cells were dissociated in EDTA, allowed to recover, and reaggregated for 60 min in media containing Fab fragments prepared from a number of antibodies. We observed no cell-cell dye transfer 4 min after microinjection in 90% of the cell pairs treated with Fab fragments of antibodies for the first or second extracellular domain of Cx43, the second extracellular domain of connexin32 (Cx32) or A-CAM. Cell-cell dye transfer was detected within 30 s in cell pairs treated with control Fab fragments (pre-immune serum, antibodies to the rat major histocompatibility complex or the amino or carboxyl termii of Cx43). We observed no gap junctions by freeze-fracture EM and no adherens junctions by thin section EM between cells treated with the Fab fragments that blocked cell-cell dye transfer. Gap junctions were found on approximately 50% of the cells in control samples using freeze-fracture EM. We demonstrated with reaggregated Novikoff cells that: (a) functional interactions of the extracellular domains of the connexins were necessary for the formation of gap junction channels; (b) cell interactions mediated by A-CAM were required for gap junction assembly; and (c) Fab fragments of antibodies for A-CAM or connexin extracellular domains blocked adherens junction formation.

Animals↗
PubMed1992

Regulation of oxygen consumption in fast- and slow-twitch muscle.

Phosphorus nuclear magnetic resonance spectra and steady-state O2 consumption rates were obtained from ex vivo arterially perfused cat biceps brachii (fast twitch) and soleus (slow twitch) muscles during and after periods of isometric twitch stimulation at 30 degrees C. In the biceps muscles, steady-state O2 consumption increased and phosphocreatine (PCr) concentration decreased progressively with stimulation. PCr recovery after these stimulation periods followed first-order kinetics with a half time of 10 min. The results in the biceps could be explained by a feedback control of cellular respiration by ADP concentration. In the soleus, steady-state O2 consumption also increased and PCr concentration decreased as stimulation rates increased. The half time for PCr recovery in the soleus was approximately 5 min, but, in contrast to the pattern in the biceps, the kinetics was not first order. There was an overshoot during the recovery period in the PCr content of soleus and a corresponding undershoot of Pi compared with resting values. Mitochondrial regulation by ADP is not sufficient to account for respiratory control in slow-twitch soleus. The respiration rate in neither muscle was dependent on the Pi content. Thus we conclude that the mechanism of control of cellular respiration is both quantitatively and qualitatively different in fast- and slow-twitch skeletal muscle.

Adenosine Diphosphate↗
PubMed1992

Renal phosphate transport and vitamin D metabolism in X-linked hypophosphatemic Gy mice: responses to phosphate deprivation.

Two closely linked, nonallelic genes, Gy and Hyp, result in X-linked hypophosphatemia in mice. The present studies in Gy mice were undertaken to determine whether renal brush-border membrane Na(+)-phosphate cotransport kinetics and adaptive responses of renal phosphate transport and vitamin D metabolism to phosphate deprivation are comparable in the two mutant strains. Transport studies in purified brush-border membrane vesicles over a phosphate concentration range of 10-500 microM demonstrated that the apparent maximum velocity of the high affinity transport system is significantly decreased in Gy mice (420 +/- 110 vs. 710 +/- 100 pmol/mg protein.6 sec, Gy vs. normal; mean +/- SE; P less than 0.05), whereas the affinity of the cotransporter for phosphate is unchanged (apparent Km, 25 +/- 3 vs. 27 +/- 2 microM; NS). Feeding a low phosphate diet results in a significant fall in plasma phosphate and an increase in brush-border membrane Na(+)-phosphate cotransport in both normal (568 +/- 40 to 1416 +/- 139 pmol/mg protein.6 sec; P less than 0.01) and Gy mice (407 +/- 27 to 1236 +/- 132 pmol/mg protein.6 sec; P less than 0.01). While the low phosphate diet elicited a rise in plasma 1,25-dihydroxyvitamin D in normal mice (51 +/- 12 to 158 +/- 12 pM; P less than 0.01), a fall in plasma hormone levels was evident in phosphate-deprived Gy mice (90 +/- 22 to 23 +/- 11 pM; P less than 0.01). Phosphate deprivation decreased 25-hydroxyvitamin D-24-hydroxylase (24-hydroxylase), the first enzyme in the renal vitamin D catabolic pathway, in normal mice (117 +/- 21 to 69 +/- 8 fmol/mg protein.min), but increased enzyme activity in Gy mice (172 +/- 14 to 240 +/- 18 fmol/mg protein.min; P less than 0.05). Moreover, under both dietary conditions, 24-hydroxylase activity was significantly elevated in Gy mice. The present results demonstrate that hypophosphatemia in Gy mice can be attributed to a decrease in the maximum velocity of the high affinity Na(+)-phosphate cotransport process in renal brush-border membranes. Our results also show that while renal brush-border membrane phosphate transport is appropriately modulated by phosphate in Gy mice, phosphate regulation of vitamin D metabolism is apparently impaired in the mutant strain. The present findings provide evidence for phenotypic similarities between murine Gy and Hyp mutations.

Animals↗
PubMed1992

The effects of bradykinin and sequence-related analogs on the response properties of cutaneous nociceptors in monkeys.

The endogenous peptide bradykinin is found in plasma and inflammatory exudates and has been implicated as a chemical mediator of inflammatory pain and hyperalgesia. Two subtypes of bradykinin receptors, B1 and B2, have been described, and antagonists for the receptor subtypes have been synthesized. The bradykinin analogs [desArg9,Leu8]BK and DArg[Hyp3,DPhe7]BK have been reported to have antagonist activity at the B1 and B2 bradykinin receptors in smooth muscle, respectively. Behavioral studies in rats indicate that the bradykinin analogs can block the algesic effects of bradykinin. We wished to determine the effects of bradykinin and the bradykinin analogs (B1 and B2 analogs, respectively) on cutaneous nociceptors in the monkey. In addition, we wished to determine the type of bradykinin receptor that mediates the sensitizing effects of bradykinin. Recordings were made from single C-fiber and A-fiber nociceptive afferents (CMHs and AMHs) that innervated hairy skin. Heat sensitivity before and after the injections was determined with a heat test sequence consisting of stimuli that ranged, in 1 degree C increments, from 41 degrees to 49 degrees C. Intradermal injections of vehicle (neutral normal saline) failed to alter the heat response of CMHs. Bradykinin (10 nmol in 10 microliters) evoked activity in 6 of 10 CMHs and sensitized all the fibers to heat stimuli. After the bradykinin injection, the mean heat threshold of the CMHs decreased from 44 +/- 0.5 degrees to 42.7 +/- 0.5 degrees C (mean +/- SEM, p less than 0.02), and the total response to the heat test sequence increased by 87% (p less than 0.002). In a related psychophysical study in human volunteers, the same dose of bradykinin resulted in a comparable (115%) increase in ratings of pain (Manning et al., 1991). Bradykinin also evoked activity in 10 of 17 AMHs and sensitized 8 AMHs to heat stimuli. Bradykinin failed to alter the threshold for activation of CMHs to mechanical stimuli as measured by application of von Frey hairs to the receptive field. In contrast to bradykinin, intradermal injection of the B1 and B2 analogs (10 nmol in 10 microliters) evoked activity in 2 of 6 and 0 of 5 CMHs, respectively. A noteworthy finding was that both analogs enhanced the response of CMHs to heat stimuli by 50% (B1 analog, 1.5 +/- 0.1; B2 analog, 1.5 +/- 0.2). The B1 (n = 10) and B2 (n = 5) analogs did not evoke activity in any of the 15 AMHs tested.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1992

Prevalence of anti-HCV in cryptogenic cirrhosis in a suburban Detroit community.

To assess the role of the hepatitis C virus in patients with unexplained chronic liver disease, we tested for the presence of anti-hepatitis C antibody (anti-HCV) in the stored serum of patients with cryptogenic cirrhosis and a variety of other chronic liver diseases. The anti-HCV assay was performed by both the enzyme-linked and recombinant immunoblot methods in 16 patients with cryptogenic cirrhosis. Eight of these 16 patients (50%) were seropositive. Six of these eight patients were born outside of the United States, compared with only one of eight seronegative patients (p = 0.021). Of the anti-HCV-positive cryptogenic cirrhotic patients, 50% also had markers of previous hepatitis B infection, compared with only 12.5% of seronegative patients. Evidence of anti-HCV positivity was found in 10%, 19%, 0%, and 0% in patients with alcoholic cirrhosis, autoimmune hepatitis, primary biliary cirrhosis, and primary sclerosing cholangitis, respectively. We conclude that in a suburban American population, hepatitis C accounts for a significant percentage of patients with presumed cryptogenic cirrhosis. Unrecognized risk factors may account for a higher prevalence of HCV in foreign-born patients with cryptogenic cirrhosis. A low prevalence of anti-HCV positivity is found in other forms of chronic liver disease.

Adolescent↗
PubMed1992

Adaptations to unilateral lower limb suspension in humans.

This study examined the effect of unilateral lower limb suspension (ULLS) on neuromuscular function in humans. Eight subjects (31 +/- 4 years old) performed all ambulatory activity on crutches for 6 weeks while wearing a shoe with a 10-cm sole on the right foot to unweight the left lower limb. Knee extensor (KE) torque during eccentric, concentric, and isometric actions, and electromyography (EMG) of m. vastus lateralis (m. VL), m. gastrocnemius medialis (m. GM) and m. soleus (m. SL) during isometric actions were assessed pre-ULLS, post-ULLS, and after 4 d of recovery. Average muscle cross-sectional area (CSA) of the KE was measured pre- and post-ULLS and that of the ankle extensors (AE) post-ULLS using magnetic resonance imaging. Strength of the KE of the suspended left limb was reduced (p less than 0.05) 21 and 15%, respectively, after ULLS and 4 d later. Average muscle CSA of the left KE decreased (p less than 0.05) 16%. The KE of the non-suspended right limb showed no changes in muscle CSA. Thus, average muscle CSA of the KE of the suspended limb was 17% less (p less than 0.05) than that of the non-suspended limb. Average muscle CSA of the AE, likewise, was smaller (18%, p less than 0.05) in the left than right leg after ULLS. Maximal integrated EMG of VL and overall mean power frequency of GM and SL for submaximal isometric actions were both decreased (p less than 0.05) post-ULLS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1991

Effect of digoxin on contractility and symptoms in infants with a large ventricular septal defect.

The effect of digoxin on contractility and symptoms in infants with a large ventricular septal defect (VSD) is controversial. Nineteen infants with symptoms of congestive heart failure due to a VSD were studied with load-independent indexes during 4 study periods: (1) before any medication; (2) while on chronic diuretics; (3) while on both diuretics and digoxin; and (4) while on diuretics alone, to determine if digoxin: (a) increases "contractility" when added to diuretic therapy; and (b) improves symptoms. Symptoms, signs (heart and respiratory rates, and weight gain), shortening fraction, preload (left ventricular end-diastolic dimension), afterload (left ventricular end-systolic wall stress) and contractility were measured at each period. The difference between the measured and predicted velocities of circumferential fiber shortening for the measured left ventricular end-systolic wall stress served as an index of contractility. Eighteen infants also underwent catheterization. Mean pulmonary-to-systemic blood flow ratio was 3:1. When digoxin was added to diuretics, contractility index was significantly greater than in control subjects (0.13 +/- 0.15 vs 0.0 +/- 0.12 circ/s, p = 0.04). When patients were again on diuretics alone (after discontinuation of digoxin), contractility index was no longer different. Symptoms and signs were not significantly improved by either diuretics or digoxin. It is concluded that in infants with a large left-to-right VSD shunt and receiving digoxin and diuretics, contractility index was significantly greater than in control subjects. However, neither diuretics alone nor in combination with digoxin improved symptoms significantly.

Digoxin↗
PubMed1991

Age-related variation in contractility estimate in patients less than or equal to 20 years of age.

The relation between velocity of circumferential fiber shortening (VCF) and wall stress (WS) is being used to estimate contractile state in a variety of disease states and patient ages more frequently. However, its relation to age has not been established. To determine reproducibility and age and sex dependence of this relation, 204 normal children (113 boys, 91 girls) underwent echographic determination of VCF and WS. The children were enrolled in 3 groups: group 1 less than 6 months old (n = 27); group 2 greater than 6 months and less than 3 years old (n = 38); and group 3 greater than 3 and less than 20 years old (n = 139). Twenty-five children also underwent serial echocardiography (n = 44) to determine reproducibility of the relation. Only 1 of the 44 repeat data pairs of VCF and WS was outside the 95% confidence limits of that relation. In all 3 groups, VCF was significantly inversely and linearly related to WS (p less than 0.001). The regression equation in the oldest group was very similar to previous reports (VCF = -0.0031 [WS] + 1.21). The regression lines in the 2 younger groups were significantly steeper and had a significantly higher y-intercept (p less than 0.01). Group 1 had the steepest slope and highest y-intercept. There was no difference in the regression lines of different sexes in any of the patient groups. It is concluded that the relation of VCF to WS is reproducible over time. It is age-dependent but has no relation to gender. VCF in patients less than 6 months old is more highly dependent on WS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Mechanically insensitive afferents (MIAs) in cutaneous nerves of monkey.

A problem in the study of nociceptors is that intense stimuli are used to locate the receptive field (RF), and thus the receptor may be damaged before the first responses are recorded. In addition, some nociceptors do not respond to the mechanical stimuli often used to search for the RF. To overcome these problems, an electrical search technique was developed to locate the RF of cutaneous nociceptors. In the hairy skin of anesthetized monkey, we used this technique to locate the RF of 63 A delta-fibers and 22 C-fibers that had extremely high thresholds or were unresponsive to mechanical stimuli. We refer to these afferents as mechanically insensitive afferents (MIAs). Ten A delta-fiber MIAs had a short latency response to stepped heat stimuli and could be responsible for first pain sensation. Five A delta-fiber MIAs and one C-fiber MIA did not respond to mechanical or heat stimuli but did respond to injection into the electrical RF of an artificial inflammatory soup containing histamine, bradykinin, prostaglandin E1, and serotonin. These chemoreceptors might be responsible for the pain and itch sensations that result from chemical stimuli. Some MIAs became more responsive to mechanical stimuli after injection into the RF of the inflammatory soup and, thus, may contribute to the hyperalgesia to mechanical stimuli associated with cutaneous injury. A large proportion of the A delta-fiber (48%) and C-fiber (30%) afferents in this study were insensitive to mechanical stimuli. The role of these MIAs in sensation needs to be studied further. The electrical search technique enables a systematic study of these afferents to be performed. This technique may also be of use to identify and characterize dorsal horn neurons that have inputs from MIAs.

Action Potentials↗